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PubMed1983

Severe fatty liver in rats fed a fat-free ethanol diet, and its prevention by small amounts of dietary arachidonate.

Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16:1/16:0 and 18:1/18:0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet.

Animals↗
PubMed2006

Effects of fatty liver and related factors on the efficacy of combination antiviral therapy in patients with chronic hepatitis C.

OBJECTIVE: Hepatic steatosis is a histological feature in patients with chronic hepatitis C (CHC) and adversely affects the virologic response rates to anti-hepatitis C virus (HCV) therapy. The aim of this study is to investigate whether the fatty liver and related factors have impact on the efficacy in CHC treated with peginterferon and ribavirin, and the associations between HCV genotyping and fatty liver. METHODS: Ninety-eight patients received subcutaneously 180 mug peginterferon alpha-2a once a week plus ribavirin. HCV genotypes and the levels of plasma insulin of patients were measured. Fatty liver was detected by B ultrasound. The body mass index (BMI), waist-to-hip ratio (WHR) and homeostasis model assessment of insulin resistance (HOMA-IR) were calculated. RESULTS: Among 98 CHC patients, 38 (38.8%) were infected with genotype 1; 44 (44.9%) with genotype 2; 13 (13.3%) with genotype 3; 3 (3.0%) with indeterminate genotype. The prevalence of fatty liver was 10.5%, 11.4%, 38.5% in patients infected with HCV genotype 1, 2, 3, respectively, which suggested that the distribution of fatty liver in different HCV genotypes was imbalanced (chi2=6.758, P=0.034). In univariate analysis, the efficacy of combination therapy was significantly associated with BMI (P=0.011), WHR (P=0.024), the levels of plasma insulin (P=0.001), genotype (P=0.036), presence of fatty liver (P=0.028), treatment dosage and duration (P=0.012) and HOMA-IR (P=0.002). With binary logistic regression analysis, the plasma insulin levels and HOMA-IR showed independent predictors to the efficacy of antiviral therapy. CONCLUSION: The prevalence of fatty liver in HCV genotype 3 was markedly higher than that of other genotypes. The BMI, WHR, the levels of plasma insulin, genotype, presence of fatty liver, treatment dosage and duration and HOMA-IR were associated with the sustained virologic response. The level of plasma insulin and HOMA-IR were independent factors for predicting effect of antiviral therapy.

Adult↗
PubMed2003

The impairment of hepatocytes and sinusoidal endothelial cells during cold preservation in rat fatty liver induced by alcohol and the beneficial effect of hepatocyte growth factor.

A fatty liver resulting from alcohol intake is often unattractive for grafting. In this study, we investigated the impairment of hepatocytes and sinusoidal endothelial cells (SECs) during cold preservation of alcohol-induced fatty liver and examined the efficacy of human recombinant hepatocyte growth factor (hrHGF). Rats were fed an alcohol diet. We performed histological examinations of the hepatocytes and observed the ultrastructural alteration of the SECs. Additionally, we measured hepatic transaminase and peroxidative lipids for hepatocellular injury and the hyaluronic acid uptake rate (HUR) to determine SEC injury. We added hrHGF to University of Wisconsin (UW) solution to assess the protective effect of the agent. Numerous fatty deposits were observed in ethanol-induced fatty livers. These grew with the duration of cold storage. Hepatic transaminases of the effluents increased during cold preservation in the livers of alcohol-treated rats. Additionally, peroxidative lipids in the effluents increased during cold preservation in the livers of alcohol-treated rats, whereas they were undetectable in non-alcohol-treated rat livers. The sinusoidal endothelium had severely deteriorated in the livers of alcohol-treated rats. Further, the HUR decreased with ethanol treatment and/or cold preservation. The addition of hrHGF suppressed the increase of hepatic transaminase in the effluent of cold-preserved alcohol-treated livers. Peroxidative lipids in the same effluents were undetectable. In fatty livers, both hepatocytes and SECs received severe damage during cold preservation. Furthermore, we demonstrated that hepatocellular injury was significantly inhibited by hrHGF.

Adenosine↗
PubMed2001

Oral treatment of mule ducks with arsenicals for inducing fatty liver.

The aim of this study was to determine the dosage and the compounds of arsenic that induce fatty liver in mule ducks and also to investigate their effects on tissue residues. One hundred four ducks, 8 wk old, were randomly selected for one of six dietary treatments in Trial 1 or one of seven dietary treatments in Trial 2. Different levels of roxarsone were administrated: 0, 10, 20, 30, 40, or 50 mg/d, respectively, in Trial 1. In Trial 2, the experimental treatments were of the same level (11.36 mg/d) with different sources of arsenic that included the control without As, roxarsone (3-nitro-4-hydroxyphenylarsonic acid), arsanilic acid, phenylarsonic acid, O-nitro-phenylarsonic acid, As2O3, or As2O5. Both trials lasted 3 wk, with 1 wk on the treatment followed by 2 wk of withdrawal. Results in Trial 1 showed that a dose of 40 mg roxarsone/d increased liver weight and caused fatty liver, whereas administration of 50 mg/d was lethal. In Trial 2, administration of arsenic (11.36 mg/d) for 1 wk significantly depressed feed intake in the roxarsone, As2O3, and As2O5 groups (P < 0.05), whereas the treatment significantly decreased only live weight gain in the roxarsone group (P < 0.05). Administration of roxarsone alone increased (P < 0.05) serum cholesterol (CHOL), albumin (ALB), and total protein (TP), whereas only As2O3 among treatments significantly decreased serum triacylglycerol (TG) concentration (P < 0.05). In the roxarsone, arsanilic acid, and phenylarsonic acid groups, serum high density lipoprotein (HDL) decreased to a greater extent (P < 0.05), and arsanilic acid treatment significantly increased the very low density lipoprotein (VLDL) (P < 0.05). After 2 wk of withdrawal, liver weights and relative liver weights were heavier in the treatment groups of roxarsone, As2O3, and As2O5 as compared to the control (P < 0.05). Levels of CHOL, TG, TP, and ALB were significantly higher in the groups treated with As2O3 or As2O5 as compared to the control (P < 0.05). The roxarsone and arsanilic acid treatments significantly decreased HDL and increased VLDL in plasma (P < 0.05). The creatine kinase (CK) level in the roxarsone, As2O3, and As2O5 groups was significantly higher compared to the control group (P < 0.05). Among the As sources, roxarsone, As2O3, and As2O5 caused fatty liver in mule ducks.

Administration, Oral↗
PubMed1980

Fatty liver and sudden death. A review.

Alcoholism is associated with increased mortality from violent and nonviolent causes. The increase in nonviolent deaths is usually ascribed, at least in part, to "cirrhosis." In the majority of these deaths this implies fatty liver rather than true Laennec's cirrhosis. Studies of sudden nonviolent deaths illustrate the largely unrecognized and frequent occurrence of sudden death with autopsy findings limited solely to fatty liver. The mechanism(s) of these sudden fatty liver deaths is unknown. Several attractive theories attribute such deaths to ethanol withdrawal induced hypoglycemia or hypomagnesemia, pulmonary fat embolization from fatty liver, or other facets of the alcohol withdrawal syndrome, including ethanol dependent maladaptive derangements of neurotransmitters. All the theories of fatty liver death remain essentially untested, however, owing to uncontrolled postmortem conditions and the lack of awareness of fatty liver deaths within the scientific community.

Adult↗
PubMed1996

Thermodynamic and kinetic properties of fatty acid interactions with rat liver fatty acid-binding protein.

Fatty acid-binding protein from rat liver (L-FABP) binds 2 fatty acids (FA) per protein, in contrast to FABPs from adipocyte, heart, and intestine, for which binding and structural studies are consistent with a single FA binding site. To understand better the unique characteristics of L-FABP, we have carried out equilibrium binding and kinetic measurements of long chain FA using the fluorescent probes of free fatty acids (FFA), ADIFAB and ADIFAB2, to monitor the concentration of FFA in the reaction of FA with L-FABP. We found that the dissociation constants (Kd) ranged from about 1 nM to 4 microM, being largest for myristate at 45 degrees C and smallest for oleate at 10 degrees C, and that 2 FA were bound per L-FABP for all temperatures and FA. The binding measurements also revealed that at temperatures below 37 degrees C, affinities for the two binding sites differ by between 5- and 20-fold but as the temperature was increased, the affinities converge toward equal values. Off-rate constants (koff) were similar for all FA and for temperatures between 10 and 45 degrees C, ranged from about 0.1 s-1 to 50 s-1. Moreover, for all FA, koff values for dissociation from both the high and low affinity sites were similar, indicating that binding affinity differences at the lower temperatures reflect lower on-rates for binding to the low affinity site. The temperature at which the affinities of the two sites become equivalent depends upon the FA; higher temperatures (45-50 degrees C) are required for the unsaturated FA and myristate than for the longer chain saturated FA (<37 degrees C). This transition from different to equivalent affinity binding sites at specific temperatures reflects a nonlinear van't Hoff behavior of the high affinity site, which in turn is a reflection of large heat capacity changes (between -0.6 and -1.2 kcal K-1 mol-1) that accompany FA binding to the high affinity site. These heat capacity changes, which are unique to L-FABP, do not appear to be correlated with a significant conformational change upon ligand binding. The differences between long chain saturated and unsaturated FA suggest that the conformation of FA bound to L-FABP may differ with both FA type and temperature, and that, in comparison to other FABPs, L-FABP may have distinctly different effects on saturated and unsaturated FA metabolism.

Animals↗
PubMed1995

[Fatty liver and obesity in university students].

Obesity is often associated with coronary heart disease and metabolic disorders. In this study, the relationship between obesity and metabolic disorders and between obesity and fatty liver by ultrasonography was investigated in 307 university students (18-20 years old, men: 196, women; 111). The correlation between Body Mass Index (BMI) and the thickness of subcutaneous fat (ST) was significant between BMI and the ratio between waist and hip circumference (WHR) was more significant in male students (r = 0.838, p < 0.001) than in female students (r = 0.639, p< 0.001). The incidence of fatty liver was significantly higher in male obese students (68.6%) than in female obese students (27.3%). After adjustment for BMI, ST, WHR and sigma glucose, the mean values for serum transaminase, cholinesterase, total cholesterol, uric acid, fasting plasma insulin and sigma insulin were significantly higher in male obese students with fatty liver than in male obese students without fatty liver. The present study suggested that male obese students with fatty liver are more likely to have metabolic disorders than male obese students without fatty liver.

Adolescent↗
PubMed2002

Epidemiology of fatty liver in a hospital-based study in Taiwan.

BACKGROUND: The aim of this study was to assess the epidemiology of fatty liver in Taiwan. METHODS: We retrospectively analyzed the medical records of all patients receiving health examinations at China Medical College Hospital from January through December 2000. A total of 1,012 subjects were included for analysis. Data were analyzed using the t test, chi-square analysis, and multivariate logistic regression. RESULTS: Our cohort was comprised of 41.8% women and 58.2% men; mean age was 49.2 years. The prevalence of fatty liver was 36.9% in all subjects, and prevalence was higher in men than in women. After controlling for other covariates, the multivariate logistic regression analysis showed that the significant factors related to fatty liver were male sex, obesity, hyperglycemia, hypertriglyceridemia, elevated glutamate pyruvate transaminase level, and hyperuricemia. Elevated glutamate oxaloacetate transaminase level was negatively associated with fatty liver. CONCLUSIONS: The prevalence of fatty liver is high in Taiwan. This study establishes background data for further investigation.

Fatty Liver↗
PubMed1994

[Two cases of systemic lupus erythematosus associated with fatty liver and Basedow's disease].

We present two cases of systemic lupus erythematosus (SLE) associated with both Basedow's disease and fatty liver. The first case is a 46-year-old Japanese female who was admitted because of high fever and general fatigue. She had been diagnosed as having Basedow's disease and treated with thiamazole for over 4 years. Since thiamazole-induced lupus was unlikely because of high titer anti-nuclear antibody and anti-DNA antibody and low levels of complements, a diagnosis of SLE was made. The upper abdominal ultrasound study and the specimen obtained by liver biopsy performed before initiating steroid therapy demonstrated marked fatty liver. SLE itself is considered as an etiology of fatty liver in this case. The second case was a 25-year-old Japanese female with SLE. She had been treated with prednisolone for 13 years and was complicated with Basedow's disease 10 years later. Fatty liver was also demonstrated in this patient on ultrasonography, and was thought to be resulted from long-term steroid hormone administration.

Adult↗
PubMed2006

Fat-derived hormone adiponectin combined with FTY720 significantly improves small-for-size fatty liver graft survival.

Owing to the discrepancy between organ donation and the demand for liver transplantation, expanding the liver donor pool is of vital importance. However, marginal liver grafts, such as small-for-size and/or fatty grafts, were associated with primary graft nonfunction or poor function. Therefore, novel combination therapies to rescue small-for-size fatty liver grafts should be investigated. In this study, we applied a combination therapy using a fat-derived hormone adiponectin (anti-steatosis) plus immunomodulator FTY720 (anti-inflammatory) in a rat liver transplantation model using small-for-size fatty liver grafts, and investigated the underlying protective mechanism such as anti-steatosis, intra-graft energy metabolism, hepatic microcirculatory changes, cell signaling cascades for survival, apoptosis and inflammation. The current study demonstrated that even a single treatment of adiponectin or FTY720 improved the 7-day graft survival from 0% to 62.5% (p = 0.001). The combination therapy significantly increased the 7-day graft survival rate to 100% by remarkable attenuation of graft steatosis and acute phase inflammatory response, significant activation of cell survival Akt pathway and maintenance of intra-graft adenosine triphosphate metabolism and improvement of hepatic microcirculation. In conclusion, the fat-derived hormone adiponectin combined with FTY720 might be a novel combination drug therapy for prevention of small-for-size fatty liver graft injury.

Adiponectin↗
PubMed2006

[Evaluation of leptin receptor Lys109Arg polymorphism in patients with non-alcoholic fatty liver disease].

OBJECTIVE: To investigate whether leptin receptor Lys109Arg polymorphism influences non-alcoholic fatty liver disease. METHODS: Genomic DNA samples were extracted from blood of subjects who had received a physical examination. Genotyping was performed using oligonucleotide microarray and these fluorescence labeled PCR-amplified fragments were hybridized to allele-specific oligonucleotide probes. The relevant mutation was confirmed by sequencing analysis. RESULTS: A total of 180 subjects (109 males and 71 females) were included in the study, 117 of them had fatty liver disease and the other 63 had no liver problems and served as healthy controls. There were 144 (80%) subjects with GG genotype (Arg109Arg), 33 (18.3%) with GA genotype (Lys109Arg) and 3 (1.7%) with AA genotype (Lys109Lys). The distribution of leptin receptor Lys109Arg polymorphism had no significant difference (P > 0.05) between the fatty liver disease patients (95GG, 21GA and 1AA) and the healthy control subjects (49GG, 12GA and 2AA). The abdominal wall fat was significantly thicker in AA genotype subjects (4.1+/-0.4) cm than that in GA (2.8+/-0.6) cm and GG genotype subjects (2.7+/-0.7) cm (F = 5.197, P = 0.006). The serum cholesterol levels in AA genotype subjects (5.1+/-0.4) mmol/L was significantly lower than that in AG (25.5+/-6.9) mmol/L and GG genotype (27.2+/-8.4) mmol/L subjects (F = 8.164, P = 0.005). There were no significant differences in age, body mass index, hip circumference, waist circumference, blood pressure (BP), percentage of body fat, blood protein, triglyceride, HDL and fasting blood glucose between AA, GG and GA genotype subjects. CONCLUSION: Leptin receptor Lys109Arg polymorphism may be involved in the regulation of distribution of abdominal wall fat thickness and cholesterol metabolism. Whether leptin receptor Lys109Arg polymorphism is in any way related to fatty liver disease is still not known.

Adult↗
PubMed2005

Elevated plasma homocysteine concentrations as a predictor of steatohepatitis in patients with non-alcoholic fatty liver disease.

BACKGROUND: Although steatosis is common in patients with severe hyperhomocysteinemia due to deficiency of cystathionine beta-synthase, there are no satisfactory data on homocysteine concentrations in patients with non-alcoholic fatty liver disease. The main aim of the present study was to evaluate the clinical significance of plasma homocysteine concentrations in patients with non-alcoholic fatty liver disease. METHODS: Seventy-one non-alcoholic fatty liver disease patients, 36 patients with chronic viral hepatitis and 30 healthy persons were enrolled in the study. Homocysteine levels were measured by high-performance liquid chromatography. Insulin, folate, vitamin B(12) and lipoprotein levels were also determined in all groups. RESULTS: Homocysteine in the non-alcoholic fatty liver disease group was found to be significantly higher than other groups. Homocysteine was found to be significantly higher in the non-alcoholic steatohepatitis group when compared with simple steatosis group. A positive correlation was found between homocysteine and triglyceride, very-low-density-lipoprotein (VLDL) cholesterol, insulin, and index of insulin resistance in the non-alcoholic fatty liver disease group, and a negative correlation was found between homocysteine and folate, or vitamin B(12) in all groups. The homocysteine threshold for the prediction of steatohepatitis was 11.935 ng/mL. Furthermore; plasma homocysteine was a statistically significant predictor for severity of necroinflammatory activity in non-alcoholic steatohepatitis. CONCLUSIONS: The plasma homocysteine concentrations were significantly higher in patients with non-alcoholic fatty liver disease, while the concentrations were not affected by chronic viral hepatitis. Plasma homocysteine is a parameter for discriminating steatohepatitis from simple steatosis. Determining the plasma homocysteine concentrations may facilitate selection of steatosis patients in whom a liver biopsy should be performed.

Adult↗
PubMed1999

Morphologic alteration of hepatocytes and sinusoidal endothelial cells in rat fatty liver during cold preservation and the protective effect of hepatocyte growth factor.

BACKGROUND: Fatty liver grafts are considered to be one of the main factors of primary nonfunctioning graft in transplantation. We investigated here, the hepatic damage during cold preservation in a rat fatty liver model by ultrastructural observation, and examined the effect of human recombinant hepatocyte growth factor (hrHGF) on amelioration of the cold-preserved graft condition. METHODS: Wistar rats were fed a choline-deficient diet (CDD) for 7 days. Livers were stored in cold University of Wisconsin (UW) solution for 0, 4, and 24 hr. We evaluated the ultrastructural alteration of the hepatocytes, sinusoidal architecture, and endothelial cells (SECs) by scanning and transmission electron microscopy. Ex vivo, we measured alanine aminotransferase (ALT) in first effluent as an index of hepatocyte injury and the hyaluronic uptake rate (HUR) as that of SEC damage. We injected hrHGF into rats fed CDD for 7 days through the portal vein and also added it to the UW solution to determine whether or not the agent ameliorated the hepatic damage in cold-preserved fatty livers. RESULTS: In rats fed CDD for 7 days, the lesion occupied by fat deposits appeared to enlarge with the duration of cold preservation leading to the disarrangement of sinusoidal architecture. Furthermore, sinusoidal endothelial damage, in which gaps, blebs, microvilli, and sinusoid denudation were detected, appeared to be more severe in these livers than in the corresponding control livers. ALT significantly increased in the 4-hr cold-preserved livers of rats fed CDD for 7 days. HUR decreased with 4-hr cold preservation and/or with CDD feeding. Administration of hrHGF prevented the expansion of fatty droplets and reduced SEC injury as detected by morphological observations. Increase of ALT in first effluent was inhibited to about one fourth the level observed in the 4-hr cold-preserved livers of rats fed CDD. Moreover, HUR significantly increased with the pretreatment of hrHGF. CONCLUSION: The hepatic injury in both hepatocytes and SECs in cold-preserved fatty liver graft developed more rapidly and severely than in the corresponding controls and demonstrated a protective effect of hrHGF.

Animals↗
PubMed2006

Prevalence and risk factors of non-alcoholic fatty liver disease among Korean adults.

BACKGROUND AND AIM: Differences in the prevalence of non-alcoholic fatty liver disease (NAFLD) between Eastern and Western populations are primarily attributable to differences in definitions and biased population selection. Thus, the aim of the present study was to accurately determine the actual prevalence of NAFLD by sonography and to characterize the risk factors for NAFLD. METHODS: The present cross-sectional study was performed with data obtained from 6,648 subjects, all of whom were older than 20 years of age (3,530 men and 3,118 women). The term 'non-drinker' was applied to men who consumed less than 30 g alcohol/day and to women who consumed less than 20 g alcohol/day. Non-alcoholic fatty liver disease was defined as a sonographically detected fatty liver in the absence of viral hepatitis in a non-drinker. RESULTS: Of the 1,613 subjects who were diagnosed with sonographic fatty liver, 1,240 were non-drinkers and had no viral hepatitis. Overall, the unadjusted and age-adjusted prevalences of NAFLD were 18.7% (23% in men, 13.7% in women) and 16.1% (21.6% in men, 11.2% in women), respectively. Multivariate analysis revealed that several risk factors were profoundly associated with the prevalence of NAFLD, including obesity, insulin resistance, hyperlipidemia and hyperglycemia in both genders, as well as age, menopausal status and estrogen medication in women only. CONCLUSIONS: These results demonstrate that the prevalence of NAFLD in Korean adults, according to sonographic surveys, is comparable to that seen in more developed countries. From the perspective of increasing obesity, the high prevalence rates noted in the study may herald an increased burden of chronic liver disease in the Korean population.

Adult↗
PubMed2006

[Liver regenerative capacity after partial hepatectomy in rats with nonalcoholic fatty liver disease].

OBJECTIVE: To explore the changes of liver regeneration after partial hepatectomy on rats with nonalcoholic fatty liver disease (NAFLD) caused by a high fat diet. METHODS: One hundred Wistar rats were randomly divided into a control group (group C, n = 45), fed with normal diet, and a NAFLD group, fed with fat-rich diet (group F, n = 55). All rats had a 70% partial hepatectomy at the end of the 12th week. They were sacrificed at postoperative 0, 1, 12, 24, or 36 hours and the percentages of their regenerated liver masses were calculated. The mitosis index was measured microscopically and the changes of cell ultrastructure were observed under an electron microscope. The expression of proliferating cell nuclear antigen (PCNA) was detected using immunohistochemistry. The expression of mRNA of cyclin D1 was measured by RT-PCR. RESULTS: The light and electron microscopy showed that the hepatic sinusoids expanded at an early period after the partial hepatectomy. The mitochondria and rough endoplasmic reticulum (RER) expanded and their number increased. The mitosis index was increased. The sinusoids of the livers in group F were narrow and irregular. The nuclei were smaller and the necrotic cells increased. As compared with the control group, the mitosis index was significantly decreased (P < 0.01), and the regenerative liver weight ratio in group F was lower at postoperative 12 h, 24 h, 36 h (P < 0.01). PCNA labeling index in group F also was lower than that in group C. The peak of the PCNA in group F was later than that of the control group (P < 0.01). In group C, the mRNA of cyclin D1 peaked at the 24th hour after the partial hepatectomy, and then decreased afterwards. In group F, it was lower than that of group C at the same time (P < 0.01). CONCLUSION: After NAFLD rats had partial hepatectomies, the capacity of their liver regeneration decreased and the peak of DNA synthesis was delayed, and at the same time the morbidity of the rats increased.

Animals↗
PubMed1990

Serum apolipoproteins B and A-I and naturally occurring fatty liver in dairy cows.

Serum lipids and apolipoprotein (apo) B and A-I concentrations were determined in 164 dairy cows which had undergone liver biopsy in early lactation. The animals were divided into groups according to fatty liver severity on the basis of hepatic triglyceride content. The serum free fatty acid (FFA) concentration was higher in cows that developed fatty livers than in normal cows, and it correlated highly with liver triglycerides. Serum total cholesterol and triglyceride levels did not correlate with hepatic triglycerides. Both apo B and apo A-I levels were significantly decreased in fatty liver cows. In particular, apo B levels showed a strongly negative correlation with liver triglycerides. The present results suggest that hepatic apolipoprotein synthesis is impeded in fatty liver cows.

Animals↗
PubMed2005

Amelioration effects of traditional Chinese medicine on alcohol-induced fatty liver.

AIM: To examine the effects of traditional Chinese medicine (TCM) on alcohol-induced fatty liver in rats. TCM consists of Astragalus membranaceus, Morus alba, Crataegus pinnatifida, Alisma orientale, Salvia miltiorrhiza, and Pueraria lobata. METHODS: The rats were separated randomly into five groups. One (the CD group) was fed a control diet for 10 wk, another (the ED group) fed an ethanol-containing isocaloric liquid diet for 10 wk, and the last three (the TCM group) were fed an ethanol-containing isocaloric liquid diet for 10 wk and dosed orally with TCM (222 mg/kg.d, TCM222; 667 mg/kg.d, TCM667; and 2 000 mg/kg.d, TCM2000, respectively) weekly during the last 4 wk. RESULTS: ED group developed fatty liver according to lipid profile and liver histological findings. Compared with the control group, liver/body weight, serum triglyceride (TG) and total cholesterol (TC), liver TG and TC, serum alanine aminotransferase (ALT) and aspartic aminotran-sferase (AST) significantly increased in the ED group. Whereas, in the rats administered with TCM, liver/body weight, serum TG and TC, liver TG and TC, serum ALT and AST were significantly decreased, and the degree of hepatic lipid droplets was markedly improved compared with those in the ED group. CONCLUSION: TCM treatment causes significant reduction in alcohol-induced lipid hepatic accumulation, reversing fatty liver and liver damage, and can be used as a remedy for alcoholic fatty liver.

Alanine Transaminase↗